Oxygen consumption of the heart: Newer concepts of its multifactoral determination

doi:10.1016/0002-9149(68)90117-3

The American Journal of Cardiology

Volume 22, Issue 3, September 1968, Pages 328-336

https://doi.org/10.1016/0002-9149(68)90117-3 Get rights and content

Abstract

The development of tension and the contractile state of the myocardium are the primary determinants of myocardial oxygen consumption. Recognition of these two factors and their interrelation has served to explain a number of apparent discrepancies in the literature. Other factors, including basal myocardial oxygen consumption, activation energy and external work, also contribute to the myocardial oxygen consumption, but to a relatively minor extent. An understanding of these general principles should permit a more rational consideration of the determinants of myocardial oxygen consumption and the implications of these factors in disease states.

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A major hub for energy dispensing, the heart itself has a high rate of oxygen consumption and as such is extremely sensitive to the shortage of oxygen supply, or ischemia [1].
Increased neutrophil infiltration and the ensuing inflammatory response represent a hallmark event in cardiac ischemia-reperfusion injury (IRI). It remains poorly defined how the epigenetic machinery contributes to this process.
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Our data suggest that trans-activation of PODXL by the BRG1-JMJD2B complex in endothelial cells may promote neutrophil infiltration and consequently the pathogenesis of cardiac ischemia-reperfusion injury.
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The traditional approach for minimizing myocardial dysfunction after CPB is directed towards modulation of the factors affecting myocardial energy consumption. Determinants of myocardial oxygen consumption have already been identified many years ago [13] and are summarized in Table 2. Starting from this perspective, it is logical that the first step in the protection against myocardial ischemia during CPB is by decreasing the three main determinants of myocellular oxygen utilization: heart rate, contractility, and intramyocardial tension development.
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I <inf>f</inf> Inhibition in Cardiovascular Diseases
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Coronary blood flow occurs mostly during diastole because the coronary vasculature has one particular property: it is compressed by the contracting myocardium such that no flow occurs during systole. In normal myocardium, tachycardia increases myocardial oxygen demand (Sonnenblick et al., 1968), and the resulting augmentation in myocardial oxygen consumption is matched by increased coronary blood flow through metabolic coronary vasodilatation. Nevertheless, coronary blood flow per cardiac cycle is reduced, because the duration of diastole is decreased over proportionately at high HR (Colin et al., 2004).
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Available clinical data indicate that IVA could improve the management of stable angina in all patients including those treated with β-blockers. As chronic elevation of resting HR is an independent predictor of mortality, pure HR reduction by inhibition of I_f could, beyond the control of anti-anginal symptoms, improve the prognosis of CAD and heart failure; this therapeutic potential is currently under evaluation with IVA.
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Myocardial energy substrate metabolism entails a complex system of enzyme catalyzed reactions, in which the heart efficiently converts chemical to mechanical energy. The system is highly regulated and responsive to changes in workload as well as in substrate and hormone supply to the heart. Akin to the terms "contractile reserve" and "coronary flow reserve" we propose the term "metabolic reserve" to reflect the heart's capacity to respond to increases in workload. The heart's metabolic response to inotropic stimulation involves the ability to increase oxidative metabolism over a wide range, by activating the oxidation of glycogen and carbohydrate substrates. Here we review the known biochemical mechanisms responsible for those changes. Specifically, we explore the notion that disturbances in the metabolic reserve result in contractile dysfunction of the stressed heart.

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^☆: From the Cardiovascular Unit, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Mass.; From the Cardiovascular Unit, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Mass. This work was supported in part by U. S. Public Health Service Grant No. 9373-2 and in part by American Heart Association Grant No. 9171-2.

^†: From the Cardiovascular Unit, Peter Bent Brigham Hospital, and Harvard Medical School, Boston, Mass.

^‡: The Cardiology Branch, National Heart Institute, Bethesda, Md.

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Symposium on myocardial metabolismOxygen consumption of the heart: Newer concepts of its multifactoral determination☆

Abstract

Am. Heart J.

Am. J. Med.

Am. J. Cardiol.

Am. J. Med.

Am. Heart J.

Am. J. Med.

Am. J. Cardiol.

Am. J. Cardiol.

Lancet

Am. J. Cardiol.

Über den Einfluss der mechanischen Bedingungen auf die Tatigkeit und den Sauerstoffverbauch des Warmbluterherzens

Arch. exper. Path. u Pharmakol.

The position occupied by the production of heat, in the chain of process constituting a muscular contraction

J. Physiol.

The effect of various mechanical conditions on the gaseous metabolism and efficiency of the mammalian heart

J. Physiol.

On the mechanical factors which determine the output of ventricles

J. Physiol.

The relationship between the volume of the heart and its oxygen usage

J. Physiol.

The regulation of the energy output of the heart

J. Physiol.

Hemodynamic determinants of oxygen consumption of the heart with special reference to the tension-time index

Am. J. Physiol.

The relation of cardiac effort to myocardial oxygen consumption and coronary flow

Circulation Res.

Left ventricular pressurevolume relationships and myocardial oxygen consumption in the isolated heart

Circulation Res.

Pressure-volume correlates of left ventricular oxygen consumption in the hypervolumic dog

Circulation Res.

Studies on digitalis XVI. Effects on myocardial oxygen consumption

J. Clin. Invest.

Myocardial oxygen consumption in acute experimental cardiac depression

Circulation Res.

Measurement of myocardial developed tension and its relation to oxygen consumption

Am. J. Physiol.

The control of myocardial oxygen consumption: Relative influence of contractile state and tension development

J. Clin. Invest.

Myocardial oxygen consumption during ventricular contraction and relaxation

Circulation Res.

The relation between the work performed and the energy liberated in muscular contraction

J. Physiol.

The heat of shortening and the dynamic constants of muscle

A study of inotropic mechanisms in the papillary muscle preparation

J. Gen. Physiol.

Implications of muscle mechanics in the heart

Series elasticity in heart muscle: Its relation to contractile element velocity and proposed muscle models

Circulation Res.

Series elastic and contractile elements in heart muscle: Changes in muscle length

Am. J. Physiol.

Contractile element work: A major determinant of myocardial oxygen consumption

J. Clin. Invest.

Physiology of the coronary circulation

Circulation

Symposium on myocardial metabolism
Oxygen consumption of the heart: Newer concepts of its multifactoral determination☆